MSN 671 Final Exam Focus Points | Questions and
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Terms in this set (96)
· An electrical current travels down the presynaptic
neuron, releasing neurotransmitters and sending these
Classic synaptic chemical messengers to the postsynaptic neuron's
neurotransmission receptors. The receiving neuron then converts the
chemical message back into an electrical impulse or
results in a cascade of sequential chemical messages
A receptor and a channel
Ligand: a NT, drug, or hormone that binds to a
receptor
Ligand-gated ion channel
Can immediately alter the flow of ions when ligand
binds
-Ligands can fall anywhere along the agonist
spectrum to alter ion flow
Ligand: a NT, drug, or hormone that binds to a
Ligand
receptor
Pentameric (5 protein subunits): GABA-A, Nicotinic
receptors, Strychnine-sensitive glycine receptors,
Ligand-gated ion channel
5HT3 receptors
subtypes
Tetrameric (4 protein subunits): AMPA, Kainate, NMDA
, Opening and closing altered by ionic charge or
Voltage-sensitive ion voltage potential
channel
Two types: Sodium and Calcium
Essential for action potentials
Made of 4 subunits forming a central alpha pore; each
subunit is made of 6 transmembrane segments:
Sodium-charged ion -Segment 4= voltmeter
channel -Segment 5-6= ionic filter (only allows Na through)
-Between 3rd and 4th subunits= amino acid plug/pore
inactivator
Site of action of many anticonvulsants
Collects NTs from the synapse and transports them
back into the neuron for packaging and release
Monoamine: SERT, DAT, NET
Presynaptic transporter
GABA: GAT
Glutamate: EAAT
helps control alertness and arousal, stress response,
cognitive functioning, attention/focus
Norepinephrine role
Linked to fight or flight
Acetylcholine role Motivation, memory, cognitive functioning, sleep
Sleep
Melatonin role
Released from the pineal gland (increased in
darkness)
Serotonin role Sleep, mood, sexuality, appetite, pain
Reward/pleasure, executive functioning, wakefulness,
Dopamine role
learning, motor control
, Inhibitory
GABA role
Sleep, mood regulation
Histamine role inflammation, alertness/wakefulness
-During darkness, there is no input from the
retinohypothalamic tract to the suprachiasmatic
nucleus (SCN) in the hypothalamus-->Signals the
Process of melatonin
pineal gland to produce melatonin
production
-MT1 receptor then inhibits neurons in the
suprachiasmatic nucleus , decreasing the wake-
promoting actions there
· Chronic blockade of D2 receptors in the nigrostriatal
pathway (D2 receptors are normally inhibitory of the
"STOP" pathway, making it "GO"--> acute blockade
causes "STOP" to predominate, resulting in slow and
rigid Parkinsonism-like movements)
-->Receptors then upregulate, causing supersensitivity
Process causing tardive
of receptors and the opposite situation (not enough
dyskinesia with an
"STOP") and, therefore, the rapid, hyperkinetic,
antipsychotic
involuntary movements of TD)
· Late and delayed in onset (months to years of
treatment)
· Can be irreversible
· By blocking the tuberoinfundibular pathway (projects
from hypothalamus to pituitary gland), which is
How can antipsychotics
normally tonically active and inhibits prolactin release
cause breast discharge
· This blockade causes a rise in prolactin-->
galactorrhea
Answers
Save
Terms in this set (96)
· An electrical current travels down the presynaptic
neuron, releasing neurotransmitters and sending these
Classic synaptic chemical messengers to the postsynaptic neuron's
neurotransmission receptors. The receiving neuron then converts the
chemical message back into an electrical impulse or
results in a cascade of sequential chemical messages
A receptor and a channel
Ligand: a NT, drug, or hormone that binds to a
receptor
Ligand-gated ion channel
Can immediately alter the flow of ions when ligand
binds
-Ligands can fall anywhere along the agonist
spectrum to alter ion flow
Ligand: a NT, drug, or hormone that binds to a
Ligand
receptor
Pentameric (5 protein subunits): GABA-A, Nicotinic
receptors, Strychnine-sensitive glycine receptors,
Ligand-gated ion channel
5HT3 receptors
subtypes
Tetrameric (4 protein subunits): AMPA, Kainate, NMDA
, Opening and closing altered by ionic charge or
Voltage-sensitive ion voltage potential
channel
Two types: Sodium and Calcium
Essential for action potentials
Made of 4 subunits forming a central alpha pore; each
subunit is made of 6 transmembrane segments:
Sodium-charged ion -Segment 4= voltmeter
channel -Segment 5-6= ionic filter (only allows Na through)
-Between 3rd and 4th subunits= amino acid plug/pore
inactivator
Site of action of many anticonvulsants
Collects NTs from the synapse and transports them
back into the neuron for packaging and release
Monoamine: SERT, DAT, NET
Presynaptic transporter
GABA: GAT
Glutamate: EAAT
helps control alertness and arousal, stress response,
cognitive functioning, attention/focus
Norepinephrine role
Linked to fight or flight
Acetylcholine role Motivation, memory, cognitive functioning, sleep
Sleep
Melatonin role
Released from the pineal gland (increased in
darkness)
Serotonin role Sleep, mood, sexuality, appetite, pain
Reward/pleasure, executive functioning, wakefulness,
Dopamine role
learning, motor control
, Inhibitory
GABA role
Sleep, mood regulation
Histamine role inflammation, alertness/wakefulness
-During darkness, there is no input from the
retinohypothalamic tract to the suprachiasmatic
nucleus (SCN) in the hypothalamus-->Signals the
Process of melatonin
pineal gland to produce melatonin
production
-MT1 receptor then inhibits neurons in the
suprachiasmatic nucleus , decreasing the wake-
promoting actions there
· Chronic blockade of D2 receptors in the nigrostriatal
pathway (D2 receptors are normally inhibitory of the
"STOP" pathway, making it "GO"--> acute blockade
causes "STOP" to predominate, resulting in slow and
rigid Parkinsonism-like movements)
-->Receptors then upregulate, causing supersensitivity
Process causing tardive
of receptors and the opposite situation (not enough
dyskinesia with an
"STOP") and, therefore, the rapid, hyperkinetic,
antipsychotic
involuntary movements of TD)
· Late and delayed in onset (months to years of
treatment)
· Can be irreversible
· By blocking the tuberoinfundibular pathway (projects
from hypothalamus to pituitary gland), which is
How can antipsychotics
normally tonically active and inhibits prolactin release
cause breast discharge
· This blockade causes a rise in prolactin-->
galactorrhea
